Session: SAT 806-823-Gestational Diabetes
Poster Board SAT-811
Deanna Dawson, Julia Wenger, Ravi Thadhani, Drucilla J. Roberts,* Rhonda Bentley-Lewis
Background: The human placenta is the critical organ responsible for the transfer of blood, nutrients, oxygen, and waste between the mother and fetus. Because the placenta shares the metabolic milieu of both mother and fetus, maternal disease can manifest in placental pathology. However, implications for maternal cardiovascular disease (CVD) risk subsequent to placental pathology have not been elucidated.
Objective: To investigate the association of specific placental pathology in women with gestational diabetes mellitus (GDM) with subsequent maternal CVD risk and to determine if race/ethnicity modifies these associations.
Methods: Study participants were selected from the MGH pathology archives between January 1, 2001 and December 31, 2009 using search terms “placenta,” “gestational diabetes,” and “GDM”. From the initial 765 placental specimens identified, we selected 129 placenta from singleton, full-term, live births whose mothers had Carpenter-Coustan-defined GDM and complete clinical/demographic data. Race/ethnicity was self-reported. CVD risk outcomes included essential hypertension and type 2 diabetes (T2D). Placental diagnoses scored included villous maturation, fetal and maternal inflammation, villous edema, and chorangiosis. Placental pathology was re-reviewed by co-authors DJR and DD blinded to race/ethnicity and prior pathologic diagnoses.
Results: Of the 129 women, 48 were white, 51 were Hispanic, 14 were Asian, 4 were black, and 14 were classified as other/unknown (excluded from analysis). The women were followed for a median of 4.1 (range 0.0-8.9) years from delivery to CVD risk outcome. Because of the limited number of non-Hispanic minority women, we aggregated the women into white and non-white groups. The non-white women had lower first prenatal visit systolic blood pressure (108 ± 10 vs. 116 ± 13 mmHg; p = 0.0004); were less likely to self-identify as a past or current smoker (8.7 vs. 35.4%; p =0.003); but were more likely to develop T2D (34.8 vs. 12.5%; p = 0.01) than the white women. Regarding placental pathology, the only significant difference was that non-white women had less chorangiosis than did white women (52.1 vs. 31.9%; p = 0.03).
Conclusion: Although more non-white women developed T2D, more white women had chorangiosis. This inconsistency may have been due to the greater percentage of past/current smokers among white compared to non-white women; however, the degree of insulin use during pregnancy warrants consideration. Further study is necessary to investigate the relationship between chorangiosis and future maternal CVD risk and race.
Nothing to Disclose: DD, JW, RT, DJR, RB
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